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Olfactory Mucosa (olfactory + mucosa)
Selected AbstractsCell surface glycoconjugates in the olfactory system of lungfish Protopterus annectens OwenACTA ZOOLOGICA, Issue 2 2000Valeria Franceschini Abstract Franceschini, V. Lazzari, M. and Ciani, F. 2000. Cell surface glycoconjugates in the olfactory system of lungfish Protopterus annectens Owen. ,Acta Zoologica (Stockholm) 81: 131,137 Lectin binding was performed on the olfactory system of lungfish Protopterus annectens to identify specific glycoconjugates on the cell surface of olfactory receptor cells. The lectin histochemical patterns and the Western blot analysis indicate that the receptor cells of the olfactory mucosa are characterized by high density of ,-N-acetyl- d -galactosamine residues on the saccharidic chains of the surface glycoproteins. Other lectins display a regional pattern between the regions of the olfactory bulbs. This different histochemical lectin pattern might be due to a different regional segregation of the olfactory projections. On the other hand it could allow the identification of an area corresponding to the accessory olfactory bulb of terrestrial vertebrates in the ventrolateral region of Protopterus olfactory bulb. The presence in the dipnoan olfactory system of a vomeronasal organ homologous to the organ in amphibians is discussed. Moreover, the selective lectin binding on the surface of primary olfactory neurones suggests that specific cell surface glycoproteins may have a role in the axonal growth due to the continuous cycle of proliferation and the death of olfactory receptor cells. [source] Contrasting effects of basic fibroblast growth factor and epidermal growth factor on mouse neonatal olfactory mucosa cellsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2007Perrine Barraud Abstract Basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) affect proliferation and survival of many cell types, but their role in the maintenance of olfactory mucosa cells remains unclear. In the neonatal mouse olfactory mucosa, cell proliferation mainly occurs in the neuroepithelium and, to a lesser extent, in the lamina propria. To establish whether bFGF and EGF affect proliferation and/or survival of these cells, we isolated olfactory mucosa cells from the neonatal mouse and cultured them as free-floating spheres under bFGF or EGF stimulation. Our data demonstrate that bFGF is a mitogen for the rapidly dividing cells (olfactory neuronal precursors and olfactory ensheathing cells), and also a survival factor for both slowly and rapidly dividing cells of the olfactory mucosa. In contrast, EGF appears to be primarily a survival factor for both the olfactory stem and precursor cells. [source] Calponin is expressed by fibroblasts and meningeal cells but not olfactory ensheathing cells in the adult peripheral olfactory systemGLIA, Issue 2 2007Chrystelle Ibanez Abstract Olfactory ensheathing cells (OECs), the principal glial cells of the peripheral olfactory system, have many phenotypic similarities with Schwann cells of the peripheral nervous system. This makes reliably distinguishing these two cells types difficult, especially following transplantation into areas of injury in the central nervous system. In an attempt to identify markers by which these two cells types can be distinguished, a recent proteomic analysis of fetal OECs and adult Schwann cells identified the actin-binding protein calponin as a potential marker expressed by OECs but not Schwann cells. Since many studies designed with the translational goal of autologous transplantation in mind have used adult OECs, this study examined the expression of calponin by adult OECs, both in vivo within the peripheral olfactory system and in vitro. Calponin colocalized with strongly fibronectin positive fibroblasts in the olfactory mucosa (OM) and meningeal cells in the olfactory bulb (OB) but not with S100, or neuropeptide-Y positive OECs. In tissue culture, calponin was strongly expressed by fibronectin-expressing fibroblasts from OM, sciatic nerve and skin and by meningeal cells from the OB, but not by p75NTR - and S100,-expressing OECs. These data, supported by Western blotting, indicate that calponin can not be used to distinguish adult OECs and Schwann cells. © 2006 Wiley-Liss, Inc. [source] Dehydroepiandrosterone regulates astroglia reaction to denervation of olfactory glomeruliGLIA, Issue 3 2004Zsófia Hoyk Abstract Effects of dehydroepiandrosterone (DHEA) on glial reactions of the peripherally denervated olfactory bulb were studied in adult male rats. Denervation was achieved by destroying the olfactory mucosa with ZnSO4 (0.17 M) irrigation of the nasal cavities. In one series of experiments, chronic DHEA treatment was applied (daily injections for 7 days, i.p., 10 mg/kg b.w. and 25 mg/kg b.w.); in the other series of experiments, animals received a single injection of DHEA (i.p., 10 mg/kg b.w., 25 mg/kg b.w. and 50 mg/kg b.w.) 2 h following ZnSO4 treatment. To determine whether DHEA conversion to estradiol was involved in the mechanism of DHEA action on glia, a third series of experiments was carried out in which the aromatase inhibitor fadrozole (4.16 mg/ml) was administered using subcutaneously implanted osmotic minipumps. Rats were killed on day 7 after chemical denervation, and the reaction of glial cells was monitored within the olfactory bulb, using GFAP and vimentin immunohistochemistry. Qualitative changes in GFAP expression were analyzed by Western blot. Chronic DHEA treatment with both doses (10 mg/kg b.w. and 25 mg/kg b.w.) and acute DHEA treatment with the highest dose applied (50 mg/kg b.w.), inhibited the increase in GFAP expression induced by the denervation of the olfactory bulb. Furthermore, GFAP and vimentin immunostaining in the glomerular layer of the olfactory bulb were diminished in the denervated and DHEA treated groups. However, when DHEA treatment was combined with fadrozole administration, such a decrease in GFAP expression could not be detected in the chemically denervated olfactory bulb. These findings indicate that DHEA, depending on the dose applied and the mode of administration, attenuates glial reaction to denervation and may regulate glial plasticity in the olfactory glomeruli. These effects are likely to be mediated at least in part by the conversion of DHEA to estradiol. © 2004 Wiley-Liss, Inc. [source] Induction of olfactory mucosal and liver metabolism of lidocaine by 2,3,7,8-tetrachlorodibenzo- p -dioxinJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 3 2002Mary Beth Genter Abstract Formulation of drugs for administration via the nasal cavity is becoming increasingly common. It is of potential clinical relevance to determine whether intranasal drug administration itself, or exposure to other xenobiotics, can modulate the levels and/or activity of nasal mucosal metabolic enzymes, thereby affecting the metabolism and disposition of the drug. In these studies, we examined changes in several of the major metabolic enzymes in nasal epithelial tissues upon exposure to the environmental contaminant 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), as well as the impact of these changes on the metabolism of a model intranasally administered drug, lidocaine. Results of these studies show that TCDD can induce multiple metabolic enzymes in the olfactory mucosa and that the pattern of induction in the olfactory mucosa does not necessarily parallel that which occurs in the liver. Further, increases in enzyme levels noted by Western blot analysis were associated with increased activities of several nasal mucosal enzymes as well as with enhanced conversion of lidocaine to its major metabolite, monoethyl glycine xylidide (MEGX). These results demonstrate that environmental exposures can influence the levels and activity of nasal mucosal enzymes and impact the pharmacology of drugs administered via the nasal route. © 2002 Wiley Periodicals, Inc. J Biochem Mol Toxicol 16:128,134, 2002. DOI 10.1002/jbt.10032 [source] A subpopulation of nervus terminalis neurons projects to the olfactory mucosa in Xenopus laevisJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2001Joseph M. Koza Abstract Biocytin application to the normal or zinc sulfate-treated nasal cavity of Xenopus laevis was used to trace retrogradely neurons associated with the terminal nerve (TN). Immunocytochemistry was conducted to identify the relationship of gonadotropin-releasing hormone-immunoreactive (GnRH-ir) TN neurons with biocytin-labeled neurons. Neurons that accumulated biocytin were located in olfactory nerve fascicles close to the olfactory mucosa lining the caudal, medial, and rostral walls of the principal cavity. GnRH-ir fibers were observed only in the olfactory nerve fascicle projecting to the rostral edge of the principal cavity. In addition, GnRH-ir fibers did not contact biocytin-labeled TN neurons. We hypothesize that these two classes of neurons represent separate components of the TN. J. Neurosci. Res. 66:8,15, 2001. © 2001 Wiley-Liss, Inc. [source] Hypothetical pathophysiology of acute encephalopathy and encephalitis related to influenza virus infection and hypothermia therapyPEDIATRICS INTERNATIONAL, Issue 2 2000Shumpei Yokota AbstractBackground: To establish a treatment strategy for acute encephalopathy and encephalitis associated with influenza virus infection, the pathophysiology of the disease was investigated through manifestations and laboratory findings of patients. Patients and Methods: A child with central nervous system (CNS) complications during the course of influenza virus infection was analyzed in view of immunologic abnormalities. In addition, four children with acute encephalopathy and encephalitis were enrolled in the hypothermia treatment for the purpose of stabilizing the cytokine storm in the CNS. Results: The CNS symptoms preceded the systemic progression to the failure of multiple organs (MOF) and disseminated intravascular coagulopathy (DIC). The mild hypothermia suppressed the brain edema on computed tomography (CT) scanning and protected the brain from the subsequent irreversible neural cell damage. Conclusion: The replicated viruses at the nasopharyngeal epithelium may disrupt the olfactory mucosa and gain access to the brain via the olfactory nerve system. The direct virus,glial cell interaction or viral stimulation of the glial cells induces the production and accumulation of the pro-inflammatory cytokines, especially tumor necrosis factor (TNF)-,, in the CNS. The cytokine storm results in neural cell damage as well as the apoptosis of astrocytes, due to the TNF-,,induced mitochondrial respiratory failure. The disruption of the blood,brain barrier progresses to the systemic cytokine storm, resulting in DIC and MOF. Mild hypothermia appears promising in stabilizing the immune activation and the brain edema to protect the brain from ongoing functional, apoptotic neural and glial damage and the systemic expansion of the cytokine storm. [source] Distribution of olfactory epithelium in the primate nasal cavity: Are microsmia and macrosmia valid morphological concepts?THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 1 2004Timothy D. Smith Abstract The terms "microsmatic" and "macrosmatic" are used to compare species with greater versus lesser olfactory capabilities, such as carnivores compared to certain primates. These categories have been morphologically defined based on the size of olfactory bulb and surface area of olfactory epithelium in the nasal fossa. The present study examines assumptions regarding the morphological relationship of bony elements to the olfactory mucosa, the utility of olfactory epithelial surface area as a comparative measurement, and the utility of the microsmatic concept. We examined the distribution of olfactory neuroepithelium (OE) across the anteroposterior length of the nasal fossa (from the first completely enclosed cross-section of the nasal fossa to the choanae) in the microsmatic marmoset (Callithrix jacchus) compared to four species of nocturnal strepsirrhines (Otolemur crassicaudatus, O. garnetti, Microcebus murinus, and Cheirogaleus medius). Adults of all species were examined and infant C. jacchus, O. crassicaudatus, M. murinus, and C. medius were also examined. All specimens were serially sectioned in the coronal plane and prepared for light microscopic study. Distribution of OE across all the turbinals, nasal septal surfaces, and accessory spaces of the nasal chamber was recorded for each specimen. The right nasal fossae of one adult C. jacchus and one neonatal M. murinus were also three-dimensionally reconstructed using Scion Image software to reveal OE distribution. Findings showed OE to be distributed relatively more anteriorly in adult C. jacchus compared to strepsirrhines. It was also distributed more anteriorly along the nasal septal walls and recesses in neonates than adults. Our findings also showed that OE surface area was not a reliable proxy for receptor neuron numbers due to differing OE thickness among species. Such results indicate that nasal cavity morphology must be carefully reconsidered regarding traditional functional roles (olfaction versus air conditioning) assigned to various nasal cavity structures. At present, the microsmatic concept itself lacks a basis in nasal chamber morphology, since OE may have varying patterns of distribution among different primates. © 2004 Wiley-Liss, Inc. [source] Odorants as cell-type specific activators of a heat shock response in the rat olfactory mucosaTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2001Virginian McMillan Carr Abstract Heat shock, or stress, proteins (HSPs) are induced in response to conditions that cause protein denaturation. Activation of cellular stress responses as a protective and survival mechanism is often associated with chemical exposure. One interface between the body and the external environment and chemical or biological agents therein is the olfactory epithelium (OE). To determine whether environmental odorants affect OE HSP expression, rats were exposed to a variety of odorants added to the cage bedding. Odorant exposure led to transient, selective induction of HSP70, HSC70, HSP25, and ubiquitin immunoreactivities (IRs) in supporting cells and subepithelial Bowman's gland acinar cells, two OE non-neuronal cell populations involved with inhalant biotransformation, detoxification, and maintenance of overall OE integrity. Responses exhibited odor specificity and dose dependency. HSP70 and HSC70 IRs occurred throughout the apical region of supporting cells; ubiquitin IR was confined to a supranuclear cone-shaped region. Electron microscopic examination confirmed these observations and, additionally, revealed odor-induced formation of dense vesicular arrays in the cone-like regions. HSP25 IR occurred throughout the entire supporting cell cytoplasm. In contrast to classical stress responses, in which the entire array of stress proteins is induced, no increases in HSP40 and HSP90 IRs were observed. Extended exposure to higher odorant doses caused prolonged activation of the same HSP subset in the non-neuronal cells and severe morphological damage in both supporting cells and olfactory receptor neurons (ORNs), suggesting that non-neuronal cytoprotective stress response mechanisms had been overwhelmed and could no longer adequately maintain OE integrity. Significantly, ORNs showed no stress responses in any of our studies. These findings suggest a novel role for these HSPs in olfaction and, in turn, possible involvement in other normal neurophysiological processes. J. Comp. Neurol. 432:425,439, 2001. © 2001 Wiley-Liss, Inc. [source] Peripheral olfactory sensitivity in rodents after treatment with docetaxel,THE LARYNGOSCOPE, Issue 4 2010Frédéric Faure MD Abstract Objectives/Hypothesis: Clinical studies have documented that cytotoxic chemotherapy is often associated with body weight loss and decreased enjoyment of food. Besides taste, olfaction plays a role in food intake. We assessed whether systemic chemotherapeutic cancer treatment compromises olfactory function in rats and mice treated with docetaxel (Taxotere; Sanofi-Aventis, Paris, France). Study Design: Randomized, controlled trials on mice and rats. Methods: Male mice received a single and male rats either a single, two, or three docetaxel administrations. Olfactory function was tested by means of electroolfactograms (EOGs) from the chemosensory epithelium of the nasal septum and the endoturbinates. We evaluated and compared the magnitude of EOG responses evoked by different odorants recorded at different time points after treatment. Results: In both animal species, docetaxel administration reduced body weight gain, thus evidencing the general toxic effect of the drug. In both animal species, the olfactory mucosa remained responsive to stimulation of odorants during the whole course of experiment, but treatment revealed regional differences of docetaxel susceptibility and induced marked transitory electrophysiological changes. In mice and rats a significant transitory decrease in EOG response magnitude occurred after a single administration. Unexpectedly, in rats we also observed an increase of the olfactory response following the second administration of the drug. Conclusions: Docetaxel exerts a neurotoxic effect on olfactory epithelia of rodents at doses similar to human doses, thus inducing transitory functional alterations. Although moderate, they are consistent with the hypothesis of a dysfunction of olfactory function. Further experiments are needed to elucidate the origin of the electrophysiological effects and their impact on the olfactory perception. Laryngoscope, 2010 [source] Pathology of the Olfactory Epithelium: Smoking and Ethanol Exposure,THE LARYNGOSCOPE, Issue 8 2004J Vent MD Abstract Objective: To investigate the effects of tobacco smoke on the olfactory epithelium. Cigarette smoking has been associated with hyposmia; however, the pathophysiology is poorly understood. The sense of smell is mediated by olfactory sensory neurons (OSNs) exposed to the nasal airway, rendering them vulnerable to environmental injury and death. As a consequence, a baseline level of apoptotic OSN death has been demonstrated even in the absence of obvious disease. Dead OSNs are replaced by the mitosis and maturation of progenitors to maintain sufficient numbers of neurons into adult life. Disruption of this balance has been suggested as a common cause for clinical smell loss. This current study will evaluate the effects of tobacco smoke on the olfactory mucosa, with emphasis on changes in the degree of OSN apoptosis. Study Design: A rat model was used to assess the olfactory epithelium after exposure to tobacco smoke. Methods: Rats were exposed to tobacco smoke alone (for 12 weeks), smoke plus dietary ethanol (for the final 5 weeks), or to neither (control). Immunohistochemical analysis of the olfactory epithelium was performed using an antibody to the active form of caspase-3. Positive staining for this form of the caspase-3 enzyme indicates a cell undergoing apoptotic proteolysis. Results: Control rats demonstrated a low baseline level of caspase-3 activity in the olfactory epithelium. In contrast, tobacco smoke exposure triggered a dramatic increase in the degree of OSN apoptosis that affected all stages of the neuronal lineage. Conclusions: These results support the following hypothesis: smell loss in smokers is triggered by increased OSN death, which eventually overwhelms the regenerative capacity of the epithelium. [source] Olfactory Neural Cells: An Untapped Diagnostic and Therapeutic ResourceTHE LARYNGOSCOPE, Issue 4 2002Christopher Perry MBBS, FRACS Abstract Objective This is an overview of the cellular biology of upper nasal mucosal cells that have special characteristics that enable them to be used to diagnose and study congenital neurological diseases and to aid neural repair. Study Design After mapping the distribution of neural cells in the upper nose, the authors' investigations moved to the use of olfactory neurones to diagnose neurological diseases of development, especially schizophrenia. Olfactory-ensheathing glial cells (OEGs) from the cranial cavity promote axonal penetration of the central nervous system and aid spinal cord repair in rodents. The authors sought to isolate these cells from the more accessible upper nasal cavity in rats and in humans and prove they could likewise promote neural regeneration, making these cells suitable for human spinal repair investigations. Methods The schizophrenia-diagnosis aspect of the study entailed the biopsy of the olfactory areas of 10 schizophrenic patients and 10 control subjects. The tissue samples were sliced and grown in culture medium. The ease of cell attachment to fibronectin (artificial epithelial basement membrane), as well as the mitotic and apoptotic indices, was studied in the presence and absence of dopamine in those cell cultures. The neural repair part of the study entailed a harvesting and insertion of first rat olfactory lamina propria rich in OEGs between cut ends of the spinal cords and then later the microinjection of an OEG-rich suspension into rat spinal cords previously transected by open laminectomy. Further studies were done in which OEG insertion was performed up to 1 month after rat cord transection and also in monkeys. Results Schizophrenic patients' olfactory tissues do not easily attach to basement membrane compared with control subjects, adding evidence to the theory that cell wall anomalies are part of the schizophrenic "lesion" of neurones. Schizophrenic patient cell cultures had higher mitotic and apoptotic indices compared with control subjects. The addition of dopamine altered these indices enough to allow accurate differentiation of schizophrenics from control patients, leading to, possibly for the first time, an early objective diagnosis of schizophrenia and possible assessment of preventive strategies. OEGs from the nose were shown to be as effective as those from the olfactory bulb in promoting axonal growth across transected spinal cords even when added 1 month after injury in the rat. These otherwise paraplegic rats grew motor and proprioceptive and fine touch fibers with corresponding behavioral improvement. Conclusions The tissues of the olfactory mucosa are readily available to the otolaryngologist. Being surface cells, they must regenerate (called "neurogenesis"). Biopsy of this area and amplification of cells in culture gives the scientist a "window to the developing brain," including early diagnosis of schizophrenia. The "Holy Grail" of neurological disease is the cure of traumatic paraplegia and OEGs from the nose promote that repair. The otolaryngologist may become the necessary partner of the neurophysiologist and spinal surgeon to take the laboratory potential of paraplegic cure into the day-to-day realm of clinical reality. [source] Scaling of the first ethmoturbinal in nocturnal strepsirrhines: Olfactory and respiratory surfacesTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 3 2007Timothy D. Smith Abstract Turbinals (scroll bones, turbinates) are projections from the lateral wall of the nasal fossa. These bones vary from simple folds to branching scrolls. Conventionally, maxilloturbinals comprise the respiratory turbinals, whereas nasoturbinals and ethmoturbinals comprise olfactory turbinals, denoting the primary type of mucosa that lines these conchae. However, the first ethmoturbinal (ETI) appears exceptional in the variability of it mucosal covering. Recently, it was suggested that the distribution of respiratory versus olfactory mucosae varies based on body size or age in strepsirrhine primates (lemurs and lorises). The present study was undertaken to determine how the rostrocaudal distribution of olfactory epithelium (OE) versus non-OE scales relative to palatal length in strepsirrhines. Serially sectioned heads of 20 strepsirrhines (10 neonates, 10 adults) were examined for presence of OE on ETI, rostral to its attachment to the nasal fossa wall (lateral root). Based on known distances between sections of ETI, the rostrocaudal length of OE was measured and compared to the length lined solely by non-OE (primarily respiratory epithelium). In 13 specimens, the total surface area of OE versus non-OE was calculated. Results show that the length of non-OE scales nearly isometrically with cranial length, while OE is more negatively allometric. In surface area, a lesser percentage of non-OE exists in smaller species than larger species and between neonates and adults. Such results are consistent with recent suggestions that the olfactory structures do not scale closely with body size, whereas respiratory structures (e.g., maxilloturbinals) may scale close to isometry. In primates and perhaps other mammals, variation in ETI morphology may reflect dual adaptations for olfaction and endothermy. Anat Rec, 2007. © 2007 Wiley-Liss, Inc. [source] | |||||||||||||